Energy availability and testosterone: why the response is not a single cutoff

A physiological outcome, not a target to maximise

EPK asks whether the relationship between food energy and body size helps explain adherence and functional capacity. Male energy-availability studies provide a way to investigate part of that question: when fuel remaining after exercise is reduced, do hormones, fatigue and performance change together?

Testosterone is one possible outcome. A change in its concentration is not a direct measurement of cellular energy, fertility or muscle growth. These studies support examining endocrine function alongside behaviour and recovery; they do not independently validate the EPK ratio.

Energy availability and EPK use different calculations

In sports research, energy availability is calculated as dietary energy intake minus exercise energy expenditure, divided by fat-free mass. Intake-based EPK divides dietary intake by total body mass. Resting expenditure per kilogram is a third quantity. A number from one calculation must not be presented as a threshold for another. [1,2]

Consider an illustrative person eating 2,000 kcal/day, expending 600 kcal/day in exercise, with body mass of 80 kg and fat-free mass of 60 kg. Intake-based EPK is 25 kcal/kg/day, but sports energy availability is about 23.3 kcal/kg fat-free mass/day. This is arithmetic, not an intake recommendation. Exercise demand could change the second value while the first stays constant.

Short trials do not produce one uniform hormone response

Koehler and colleagues studied six exercising men under four-day conditions including low energy availability of 15 kcal/kg fat-free mass/day. Leptin and insulin fell, but testosterone and T3 did not change significantly. The small sample and short exposure limit conclusions about longer restriction. Normal testosterone therefore cannot exclude every early physiological response to under-fuelling. [1]

Sim and colleagues studied 12 male endurance runners in randomized four-day conditions at 45, 30 and 15 kcal/kg fat-free mass/day. The most restricted condition reduced testosterone and increased fatigue, while other measured outcomes were largely unaffected. The finding supports following symptoms and endocrine measures together; it does not establish a universal diagnostic cutoff. [2]

Performance and well-being also matter

Jurov and colleagues reduced energy availability in stages and observed changes in performance and well-being. Their testosterone results require precision: the most restricted stage showed a non-significant trend in absolute testosterone (p=0.095), while a separate repeated-measures analysis of reference-range quartiles was significant (p=0.026). These are different endpoints. The study did not identify one threshold applying to every outcome or participant. [3]

For EPK, this suggests that waiting for one hormone to cross a laboratory boundary may miss relevant changes in function. It also prevents the opposite error: attributing every instance of fatigue to an energy deficit without considering sleep, illness, training history or other causes.

Sleep and sampling change the interpretation

A small experiment by Leproult and Van Cauter reported lower daytime testosterone after restricted sleep. Later randomized experiments did not find a clinically meaningful testosterone reduction under their tested sleep-restriction conditions. Timing, exposure and measurement methods can help explain why results differ. [4,5]

Clinical diagnosis requires compatible symptoms or signs and consistently low testosterone, confirmed with repeat morning fasting measurements under the guideline. LH and FSH help distinguish primary from secondary hypogonadism. An EPK value cannot replace that assessment or establish a reason to take hormones. [6]

How this strengthens the EPK research question

These experiments justify studying endocrine and functional responses when energy supply is constrained. The next question is whether intake-based EPK adds useful information beyond measured intake, exercise expenditure, fat-free mass, sleep and body composition.

A prospective study could record those variables before restriction and follow fatigue, adherence, performance and repeated hormone measurements over time. Prespecify the exposure and sampling conditions, then compare EPK with models that enter energy and mass separately. A reproducible additional contribution would support the framework; no added predictive value would limit the role of the ratio.

The evidence supports a context-sensitive hypothesis about energy and function. It does not establish a universal 25 kcal/kg minimum, a testosterone target, or a supplement protocol.

Related working papers

Read the relevant PDFs: EPK–001 to 007 are the revised version 1.2 papers; EPK–008 to 010 are version 1.0 supplements. Earlier PDFs and DOI records remain on the paper archive.